| External factors: | 5-MTP |
| Aging type: | Prevent |
| Aging characteristic: |
| Category: | Chemical compounds |
| Phenotype: | Aging |
| Experiment: | BrdU assay//SA-β-gal activity assay//qPCR//ELISA |
| Description: | BM-MSCs cultured in HG had a lower BrdU incorporation and pretreatment with 5-MTP alleviated the reduction. HG-induced IL-6 secretion was significantly reduced by 5-MTP pretreatment. 5-MTP did not exert a significant effect on SA-β-Gal in LG-MSCs while it significantly reduced HG-induced elevation of SA-β-Gal positive cells. Pretreatment of BM-MSCs with 5-MTP attenuated p16 and p21 expression, BrdU incorporation, IL-6 secretion, SA-β-Gal and Lysotracker-positive cells. These results indicate that 5-MTP is effective in controlling oxidant-induced premature senescence. |
| Target gene: | FOXO3A |
| R-EF-Target gene: | Upregulation |
| Official symbol(s): | FOXO3A |
| Target gene experiment: | Western blot |
| Target gene description: | 5-MTP significantly increased FoxO3a proteins in HG-MSC. |
| Regulatory pathway: | mTOR |
| R-EF-Pathway: | -- |
| Official symbol(s): | MTOR |
| Pathway experiment: | qPCR//SA-β-gal activity assay//ELISA |
| Pathway description: | To ascertain that 5-MTP inhibits senescence through mTOR, we treated BM-MSCs with rapamycin and analyzed senescence markers. Rapamycin did not have a significant effect on p16 expression in LG-MSC but abrogated the p16 lowering effect of 5-MTP in HG-MSC. Similarly, 5-MTP-induced reduction of p21 transcript was abrogated by rapamycin. Rapamycin did not influence HG-induced SA-β-Gal but abrogated the 5-MTP-mediated control of SA-β-Gal in HG-MSC. Rapamycin abrogated 5-MTP-mediated control of IL-6 in a manner similar to its abrogation of the rise of other senescence markers. |
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